Trematode
Parasites: What Is Their Genesis?

An overview of trematode1
parasitology from the evolution and creation perspectives is presented,
including a discussion of the design-like features of these
parasites. No credible evolutionary explanations are found in the evolutionary
literature to account for these design-like aspects.

Histological microtechnique
for electron microscopy is also reviewed and some cyst ultrastructural
data are reported. A caring God may have designed trematodes, now recognized
as parasites, to serve other functions before the Fall of man (Genesis
3).

Introduction

The purposes of
this study are to review some of the design-like behaviors
and structures of this group of parasites, to search for a reasonable
explanation for their existence in the evolutionary literature, and to
provide a creation-based explanation for their origins.

As shown previously
(Lumsden and Armitage, 1999), digenetic, heterophyid trematode parasitic
worms of the genus Ascocotyle infect certain amnicolid snails as
first intermediate hosts (such as Littoradinops). They also infect
certain cyprinodont and poeciliid estuarine fishes (Cyprinodon, Poecilia,
Fundulus, Gambusia), as second intermediate hosts in a three-step
life cycle. The hermaphroditic, adult trematode worms mature in the intestines
of definitive hosts, most often piscivorous birds, but also certain mammals
such as the raccoon. The Ascocotyle group comprises some 30 different
species, which vary by mostly minute morphological differences, such as
spine count and shape, organ position and size, and organ shape within
adults. They also vary in metacercarial cyst shape and thickness, location
of infection within the second intermediate host, and the specific host
type.

The cyst wall configuration,
as observed by TEM (this paper) also can serve as a diagnostic species
characteristic. It is on the basis of these morphological features and
not reproductive isolation alone that species are identified within this
group. These parasites cannot be classified on the single basis of reproductive
isolation, as many animal species are, because trematodes are hermaphroditic
and several species often inhabit the same estuary.

All of these observed
differences are considered by creationists to be at the microevolutionary
level of variation, or normal variation within a created kind. The creation
model of origins predicts small changes within a kind based on the genome
designed by the Creator at the beginning. In contrast, very large scale
genomic changes, as espoused by the evolution model of origins, would
be necessary to change the Ascocotyle worm into a cestode or an
annelid, if it could be done at all.

Some workers have
reported on the apparent pathogenicity of the Ascocotyle genus
(Martin and Steele, 1970; Snyder et al., 1989; Font, Overstreet and Heard,
1984; Font, Heard and Overstreet, 1984), but many more have shown large
numbers of parasites within infections of no pathogenicity (Stunkard and
Uzman, 1955; Burton, 1956; Lenhoff et al., 1960; Lumsden, 1963a; Schroeder
and Leigh, 1965; Skinner, 1975; Coleman, 1993; Ostrowski de Nunez, 1993)
other than occasional blood flow impediment caused by mechanical occlusion
within the heart or the circulatory system. Some significant ultrastructural
observations (Lumsden, 1968; Stein and Lumsden, 1971a, b; this paper)
using TEM, show that there is absolutely no pathogenicity or host immune
response resulting from the presence of the parasite within host tissues.
Many workers have even reported that heavily infected snails and fish
live for up to a year or more in laboratory aquaria (Leigh, 1956; Stein,
1968; Font, Heard and Overstreet, 1984, and my own observations over many
months).

There has been very
little discussion by previous workers regarding the complexity of the
Ascocotyle life cycle (which requires parasitization of three distinct
hosts for completion of its life cycle) and what mechanisms may have brought
this multifarious system into place. Most, if not all of the evolutionary
literature on digeneans in general and ascocotylids in particular fails
to develop a credible, empirically-based phylogeny for these organisms.

Some aspects of
the Ascocotyle life cycle exhibit design-like features
in behavior, morphology, and structure. These features take the form of
behaviors which guide the microscopic parasite to the appropriate host
(even in the presence of other fishes), behaviors and sensory papillae
which guide the parasite to the appropriate organ for encystment, and
specialized structures which allow tissue penetration. There are also
other complex structures which control safe passage of the parasite through
the digestive or circulatory systems of intermediate and definitive hosts
and minimize host immune response.

Workers at the University
of California Santa Barbara, have collected some of the same hosts used
in this study and have described the actual alteration of host behavior
by trematode parasites to ensure predation by the definitive host (Lafferty
and Morris, 1996). Their failure to provide an evolutionary explanation
for such a highly designed system, however, is evident. Other limited
discussions of evolution within the Ascocotyle group are offered
(Sogandares-Bernal and Lumsden, 1964; Skinner, 1975; Font, Heard and Overstreet,
1984), but no serious explanation has been proposed for how these complex
life cycles were initiated and how they arrived at their present state.

The real question
is, can parasites be designed? If they can be designed, what would constitute
a design feature and how would it be recognizable as such? If certain
features are attributed to design, can evolutionary explanations likewise
be made for them? If parasites such as Ascocotyle were designed,
can that design be attributed to a Master-Designer within a Biblical creationist
model of origins?

Implications
for Creationism

The heteroecious
life cycle of the Ascocotyle parasite is complex and it clearly
shows that it is obligated to a cycle requiring the timely intervention
of at least three different hosts for it to achieve fecundity. Many questions
are raised by such life cycles with respect to possible natural selection
or environmental pressures which may have driven the Ascocotyle
parasite (and most trematodes) to seek refuge within these very different
hosts in order to reach maturity.

There is no reference
in the ascocotylidliterature to any significant mechanism which
may account for the presence of such complex life cycles, except the usual
vague homage paid to an evolutionary parasite strategy, and/or
selective advantage. Some discussion is made in defense of
possible evolution-based parasite-host relationships (Sogandares-Bernal
and Lumsden, 1964; Yamaguti, 1971; Skinner, 1975; Font, Heard and Overstreet
1984; Lafferty and Morris, 1996), but answers are often speculative. Statements
such as Yamagutis (1971) prevail:

The present information
indicates that the adoption of the parasitic habit occurred at an extremely
remote period (of earth history) and that the evolution of parasitic life
cycles with accompanying adaptions of the parasites, has proceeded hand
in hand with the evolution of their hosts. (brackets mine).

There is no question
that worm parasitism has been a part of the biosphere since early times
(Poinar, 1984; Ferreira, et al., 1993), and in the creationist model,
it certainly pre-dates the Flood. To relegate its origins to a misty past,
however, is to avoid the obvious question: Where, when and how did it
arise?

The evolutionary-based,
trial and error method of adaptation proposed by these authors, fails
to serve as an acceptable explanation for the presence of heteroecious
life cycles and likewise falls flat in explaining the complex biochemical
and sanctuary interactions between these parasites and their hosts. Evolutionary
progression would require countless failed random experiments on the part
of a parasite to make the transition from a free-living state to life
within three completely different host environments, something that an
ascocotylid now freely enjoys. Evolution appears to fail in this regard
because it cannot be in an organisms best interest to
fetter itself to another organism, upon which it must depend
for its very survival, let alone three different organisms in multiple
habitats. Behe (1996) has shown that complex biochemical interactions
(which themselves are based upon irreducibly complex biochemical structures)
 cannot be formed on a trial and error basis. If these relationships
were designed by a Master-Planner from inception, however, then a possible
symbiotic exchange may be taking place (or occurred once in the past)
and the relationship could be explained on that basis.

Except for one brief
note in Smith (1984) describing some alteration of host behavior by parasites,
and my recent papers (Armitage, 1997a; 1998; Lumsden and Armitage, 1999),
no worker has seriously studied trematodes from a strictly creationist
viewpoint. Furthermore, there is no reference in ascocotylid literature
which states that a possible positive relationship might exist between
this group of worms and their hosts. On the contrary, these infections
are often characterized by researchers as merely being benign or minimally
harmful (Stein and Lumsden., 1971a, b; Coleman, 1993). This study represents
the first attempt to show that these heteroecious life cycles and specialized
structures are too complex to have developed by chance, and to present
a creationist design argument for the presence of such parasites.

On the other hand,
it is most difficult to account for these apparently created structures
on an evolutionary basis. The very fact that these organisms can invade
a host and go undetected by the immune system implies that certain biocompatibilites
were in place before the life cycle was initiated.

Evolutionary
Explanations forApparently Designed Features

A search of the
ascocotylid literature failed to produce a satisfactory evolutionary explanation
which can account for the complex life cycle and the design-like
structures employed within this group. One is hard-pressed to synthesize
any meaningful evolutionary rationale from this literature, particularly
in the field of host behavior modification. Comments like: a parasite
can parlay a small (host) behavioral modification into a large increase
in predation abound (Lafferty and Morris, 1996, p. 1394) (brackets
mine).

Stunkard (1946)
reviews Odhners contention that similarities in the reproductive
and excretory systems of digenetic trematodes indicate a common origin
of all digeneans but he does not elaborate further. Sogandares-Bernal
and Lumsden (1964) do not offer a mechanistic solution for the origin
or complexity of the ascocotylids, but they do state that a significant
and complex behavior of the worm to remain in the definitive host
long enough to produce, but not release a potentially dangerous (to the
host) burden of eggs may be an evolutionary adaptation by the parasite
(brackets mine). Cable (1974) does attempt a phylogenetic survey of the
trematodes, but does not focus on the digeneans or design features per
se. Skinner (1975, p. 342) contends (with little argument) that parasites
evolve slower than their hosts. He focuses on the intricate features of
ascocotylids, saying, their narrowly defined habitat and high specialization...(makes
them) good material for the exploration of evolutionary development...,
and ...similarities in the parasite fauna point to close host relationships...
(brackets mine). Overstreet (1978) suggests that the evolutionary relationships
of some fishes can be explained on the basis of the similar types of parasites
which infect them. With respect to the complexity of the life cycle, he
then states, however, The more complicated the life cycle and the
greater the variation in the stages, the more a cycle can be influenced
by the environment (Overstreet, 1993, p. 127), indicating that possibly
the environment molded the life cycle.

In a section of
their book describing the staggering complexity of digenetic trematode
eyespots, chemosensory papillae and other sensory structures, Schmidt
and Roberts (1989, p. 234) exclaim that the sensory endings (in
one larval stage) are strikingly similar to the olfactory receptors of
the vertebrate nasal epithelium! but offer no mechanism of how they
came to be that way (brackets mine). This would support a strange phylogeny
indeed!

As to why trematode
cercariae typically manifest abundantly more sense organs than the supposedly
more highly developed adults, they surmise that (this is) undoubtedly
related to the adaptive value of finding a host quickly (p. 233)
(brackets mine). The assumption here is that once the worm adapted to
finding a host by using these sense organs, the energy required to maintain
the sense organs in the adult became less adaptive than just losing them.
This is just one example in a long string of the typically imaginative
explanations offered by evolutionists, but then Schmidt and Roberts (1989,
p. 240) admit that the complexity of the life cycle has fueled the imagination
for a long time:

This alternation
of sexual and asexual generations in different hosts is one of the most
striking biological phenomena. The variability and complexity of life
cycles and ontogeny have stimulated the imaginations of zoologists for
more than 100 years, creating a huge amount of literature on the subject.
Even so, many mysteries remain, and research on questions of trematode
life cycles remains active.

With respect to
the wildly different environments this parasite must deal with as it passes
from host to host, Schmidt and Roberts (1989, p. 248) state, that they
go through a sequence of totally different habitats in which the
various stages must survive, with physiological adjustments that must
often be made extremely rapidly. There are wide swings in osmotic
pressures from host to host. The chemical nature of the host skin must
be detected. They need to penetrate host skin using leukotrienes and prostaglandins
(which are very sophisticated proteins) and they must possess a myriad
of ways to evade host immunological detection once they are on board.
Although the synthesis of these highly specific proteins and enzymes by
microscopic parasites is currently unexplainable, evolutionary authors
are reluctant to relinquish the supposed materialistic origin:

When one considers
that chance governs the successful completion of much of the life
cycle of any given parasite, it becomes apparent that the odds against
success are nearly overwhelming (Schmidt and Roberts, 1989, p. 12) (emphasis
mine).

The use of sophisticated
macromolecules by these parasites to alter host behavior is also discussed
by Lafferty and Morris (1996, p. 1395) who admit that, We know little
about the mechanisms parasites use to alter host behavior, but some evidence
exists for sophisticated manipulation of (host) hormones and neurochemicals...
(brackets mine). How this remarkable manipulative ability came about is
not discussed.

Whatever the ancestral
digenean, any system of their phylogeny must rationalize the evolution
of their complex life cycles in terms of natural selection, a most perplexing
task.

The subsequent evolutionary
reconstruction is padded with phrases like, most authorities today
believe, this may imply, it is not difficult to
imagine, it may be assumed, was probably,
it is likely that, and less difficult to visualize.
It can be seen that the origin of these parasites from an evolutionary
point of view is indeed perplexing.

With respect to
the supposed evolutionary development of symbiosis and parasitism, McLaughlin
and Cain (1983, pp. 189190) also tender some less than convincing
arguments, and frankly state that the data are scarce. They
reference just one laboratory study in which a bacterium and an amoeba
established a mutualistic relationship after 100 generations in a controlled
laboratory environment. These authors offer four general principles for
the origin of symbiosis and admit that:

Naturally, the...model
is speculative...

1) Symbioses originate
rapidly and frequently in nature. Partners evolve rapidly under the pressures
of adapting to the symbiotic relationship. Once a complete, free-living
life cycle is impossible for one of the partners, it is committed to the
evolutionary progression described.

2) One partner,
the host...eventually gains control of the relationship after it becomes
obligatory to the other partner, the symbiont.

3)The evolutionary
progress is unidirectional; the symbiont often becomes less pathogenic,
then non- parasitic, then actually beneficial to the host (if this is
possible; if the symbiont has nothing to offer, then it simply becomes
extinct).

4)Eventually, the
desirable features of the symbiont which can be incorporated by the host
are so incorporated. The symbiont becomes either extinct or a diminishing
part of the host.

To their credit,
the authors are candid about the lack of experimental support for their
logic. The problem with this kind of evolutionary scenario is that generous
anthropomorphisms are ascribed to microscopic creatures which can in no
way be self-aware. They cannot be aware of the concepts of symbiosis,
parasitism, interesting ploys, desirable features,
nothing to offer, selective advantage, etc.all
of which are teleological value judgments which are constantly and readily
made. How, indeed, can a parasite know what is in its best
interest from an evolutionary (or any) point of view? Perhaps these
authors only mean that these seemingly directed behaviors and structures
really occur as a result of natural selection in gene pools, but if that
is the case, they do not say so.

Further, the whole
idea that a microscopic trematode or other parasite can guide
its intermediate host to the actual definitive host by scheming
to alter its behavior via an evolutionary strategy is absurd.
Carney (1969) discusses the alteration of formicine ant behavior by the
lancet fluke trematode (Dicrocoelium dendriticum). He writes about
this and the liver fluke (Brachylecithum mosquensis) which ensure
their own predation by the herbivorous sheep which serves as the definitive
host. These trematodes evidently cause the ant to climb to the tips of
grass during the period when sheep graze. With no supporting material,
Carney states:

Both flukes have
parallelly evolved the ability to alter their intermediate hosts
behavior such that their own chance of survival is enhanced... Bizzare
adaptations to parasitism such as these are one of the most interesting
aspects of biology, although often the least known, and indicate a long
association between these flukes and their respective hymenopteran hosts
(p. 610).

Curio (1988) comments
on this as well, stating:

To manipulate hosts
behavior patterns seems to ask a lot in evolutionary novelties. However,
the brainworm when inducing an ant to cling to the top of plants capitalizes
on an apparently ancient behavior... the parasite needed merely
to reactivate a hidden potential of the ant (p. 151).

Moore (1984) surveys
several parasites, particularly in the acanthocephalans (spiny headed
worms), which are known to alter intermediate host behavior, and he laments:

...the parasites
do not induce novel behavior patterns but merely elicit existing patterns
at disastrously inappropriate times. Nevertheless, this is quite a feat,
and a general physiological explanation of how an acanthocephalan accomplishes
it while floating in the body cavity of the host has yet to be found.
The realization that parasites can change host behavior has intriguing
implications. Biologists observing certain animals in the field must now
take into account the possibility that the observed behavior may have
been rigged (p. 115).

Moore, however,
does not elaborate on who or what may have done the rigging.
In a discussion of host castration by parasites, Hurd (1990, p. 274) writes:

Baudoin (1974),
considered parasitic castration in the wider sense, outlined above as
an evolutionary strategy, and concluded that a parasite-induced manipulation
of host resources away from reproduction may produce increased host survival,
thus leading to increased parasite fitness as a result of an improved
environment.

In this case it
is assumed either that the parasite has understood what host
resources are and has devised a strategy to ensure
its own fitness, or that chance, natural selection, and mutation caused
it.

Aeby (1991) discusses
trematodes which encyst in coral polyps as an intermediate stage, changing
the polyp appearance and behavior. These trematodes later mature in the
definitive host, a coral-eating fish attracted by these very changes.

In the discussion,
she writes:

One might question
why fish would evolve to feed on infected polyps... I can only speculate
about this, but there are several hypothetical explanations... The parasite
residing in the fish may have adopted the prudent parasite
strategy (Holmes 1983) in which the parasite produces minimal damage to
the host (p. 267).

The fact that a
parasite induces minimal damage on its fish host hardly seems a compelling
reason for a fish to begin feeding on infected polyps in the first place!

Lafferty and Morris
(1996, p. 1390) state,Three main lines of evidence currently support
the hypothesis that behavior modification is a parasite strategy evolved
to increase transmission... The authors then go on to point out
that the very fact that increased predation by the definitive host is
occurring in conjunction with parasitism is evidence enough that such
a strategy has evolved. One clue to an evolutionary origin
for these parasites would be the discovery of a free-living variety or
finding a parasitic trematode that completed all stages of the life cycle
in one host. There is, however, only one example in the literature of
all three stages of this life cycle occurring in one host (Barger and
Esch, 2000), but there are no free-living forms. A snail is required as
a first intermediate host, followed by a fish or frog, and finally a piscivorous
bird or mammal. All digenetic heterophyid trematodes are endoparasitic
and obligated to these hosts. Why would a parasite initially become completely
dependent upon a host for its very survival? How could such a relationship
develop over time from a free-living state to a parasitic state? Why would
an Ascocotyle tie itself to such a risky developmental route, where
not one, but three hosts are required?

Overstreet (1978)
classifies all organisms which live together as symbionts. He states that
a symbiont becomes a parasite, when (it) depends entirely upon a
host, occasionally harming it... (p. 2). Commensals live together
and eat from the same table, and mutualism occurs when ...both
parties benefit and both metabolically depend on each other (Overstreet
1978, pp. 24; 1993). There is no doubt that an Ascocotyle
is a parasite and a commensal. Quite possibly it even has a metabolic
dependence upon one or more of its hosts to dissolve its cysts. Some question
remains as to whether the Ascocotyle worm is involved in a mutualistic
relationship in which it actually benefits its host. All members of this
genus have an oral coronet of large spines at the adult stage, some having
two rows, some having one row, etc. (Armitage 1997a). Of what purpose
are these spines? The adult worm appears to lodge in the intestinal mucosal
crypts of the definitive host, but does not penetrate the mucosal layer
(Font, Overstreet and Heard, 1984; Font, Heard and Overstreet, 1984).
Worms hold on in a cup-shaped fashion, over the host villi, by using both
the acetabulum and the oral sucker. Yet no pathology to the villi is observed
so the oral spines are possibly not used as holdfasts. But of what value
are two rows of spines rather than one, or of one additional incomplete
row in preference to a complete one? Why is a single incomplete row never
observed? The tegument of these worms is entirely covered with a carpet
of fine body spines which certainly must aid in anchoring the parasite
and resisting host peristalsis.

In experiments conducted
with cercaria of A. mcintoshi Price, Leigh (1974) discovered that
cercarial penetration glands are HCl-sensitive and fully evert in weak
solutions of HCl. Of what purpose is a set of penetration glands that
are activated only in the presence of HCl, glands that are required for
entry into host tissues, unless the parasite in question anticipates
the gastric juices of the fish which swallows it as the second intermediate
host? Could a trial and error method account for this elegant penetration
gland? This biochemical functional system seems to fall within Behes
(1996) category of irreducible complexity. If the sensitivity
to HCl were removed, would the parasite fail to penetrate the host tissue?
To bequeath this biocompatibility to the ancient processes of time and
chance strains ones scientific credibility to the breaking point.
One of the most compelling arguments for design within this Ascocotyle
group comes from the structure of the metacercarial cyst, which is HCl
resistant, and yet, temperature, pH and trypsin sensitive (Stein, 1968).
Without a temperature of 37o C, a solution
adjusted to pH 7.5, and the presence of trypsin, the cyst will not dissolve.
Only with this combination can the parasite, encased within its miniature
ark, successfully pass the definitive host stomach and dissolve only within
the somewhat protective confines of the intestine, which is perfectly
matched to its required conditions. Schmidt and Roberts (1989, p. 248)
observe, This combination of conditions is not likely to be present
anywhere but in the intestine of a homoiothermic vertebrate....

The evolutionary
literature has failed to supply us with a proper explanation for how these
design-like features may have come about by the chance, random
processes of evolutionary descent.

Intelligent Design Explanations

The questions which
confront us have to do with the relationships, behaviors and specialized
structures observed in this parasite  all of which appear to have
been designed (Armitage, 1998). Such designs exhibit irreducible complexity
as observed by Behe (1996) for the chemical basis of human vision and
blood clotting. Behes conclusion is that a gradualistic, Darwinian
mechanism could never have produced these features:

The impotence of
Darwinian theory in accounting for the molecular basis of life is evident
not only from the analysis in this book, but also from the complete absence
in the professional scientific literature of any detailed models by which
complex biochemical systems could have been produced...the scientific
community is paralyzed. No one at Harvard University, no one at the National
Institutes of Health, no member of the National Academy of Sciences, no
Nobel prize winnerno one at all can give a detailed account of how
the cilium, or vision, or blood clotting, or any complex biochemical process
might have developed in a Darwinian fashion (p. 187).

And:

There is an elephant
in the roomful of scientists who are trying to explain the development
of life. The elephant is labeled intelligent design. To a
person who does not feel obligated to restrict his search to unintelligent
causes, the straightforward conclusion is that many biochemical systems
were designed. They were designed not by the laws of nature, not by chance
and necessity; rather they were planned. (p.193) (emphasis in the
original).

Ascocotylids are
able to rapidly manufacture macromolecules necessary to render osmotic
potentials harmless. They can synthesize host penetration macromolecules
used for swiftly and painlessly entering their intermediate hosts. They
also produce the macromolecules which will envelop them with a immune-transparent
cyst that will not dissolve in HCl but which will come apart readily in
a warm, pH adjusted, environment, bathed in trypsin and bile salts. All
these characters demand planning just as much as does Behes blood
clotting mechanism. But the question remains of whether or not a loving
God would plan invaders such as these. Were these organisms designed from
the start to perform functions they no longer perform? Answers to these
questions may vary but we can be sure that a loving God did not intend
the rampant parasitism we observe today.

The only acceptable
alternative to the evolution explanation is that these complex life cycles
and design-like structures were planned by the Creator, at
the point in history when He designed all of the other living organisms.
Why and how some symbionts have today become pathogenic is open for speculation,
but in a creation scenario, pathobiology must certainly be related somehow
to the Fall of Adam and the subsequent Curse (Genesis 1:31; 3:18).

Delving
Deeper into TrematodeBiology: Microtechnique

In an effort to
explain the basis of this and other studies, in which TEM has been applied
to the cyst walls of trematode worms, a primer on the preparation of biological
material is presented in the appendix. The appendix and the illustrations
will also serve to orient the reader to the field of microtechnique and
to show contrasting features in Ascocotyle cysts.

The Ultrastructure
of Metacercarial Cyst Walls

At one time researchers
believed that the thick-walled metacercarial cyst of trematodes encysted
in various hosts was a direct response by the host to the presence of
the parasite within tissues (Sogandares-Bernal and Lumsden, 1964). It
now is known however, that cyst walls are produced by secretions from
the tegument of the metacercaria and may even be used to delineate differing
species based upon its unique structure (Stein and Lumsden, 1971b; Stein
and Basch, 1977). But certain other authors have not agreed that this
is a species characteristic (Huffman, 1968; Wittrock et al., 1991; Walker
and Wittrock, 1992). The extent of host response to the presence of cysts
varies considerably. The typical host response is the production of a
fibrous collagen capsule surrounding the cyst, along with associated host
fibroblasts, but there is little or no host immune response ( Lumsden,
1968; Stein and Lumsden, 1971a, b; Mitchell, 1974; Higgins et al., 1977;
Stein and Basch, 1977; Gulka and Fried, 1979; So and Wittrock, 1982; Galaktionov
et al., 1997).

The variation in
layers of cyst walls within the ascocotylids is seen in the following
examples. Ascocotyle pachycystis (Figure 1), produces a four-layered
cyst up to 35 micrometers in thickness (Stein and Lumsden, 1971b) with
two major, bilayered lamellae. A. chandleri (not shown) exhibits
a 15 micrometer-thick cyst with two layers (Lumsden, 1968). A. leighi
(Figure 2), was shown to have a 10 to 11 micrometer thick cyst which also
has two layers (Stein and Lumsden, 1971a). The cysts of A. tenuicollis
(Figure 3), collected in Mississippi come closer in structure to A.
chandleri than any other member of this genus because of a three-layered,
nine micrometer-thick cyst. A. sexidigita has a 16 micrometer-thick,
three layered cyst (not shown). A. (P.) diminuta has a single cyst
wall of 1.5 to 3 micrometers in width (Figure 4), which in every respect
resembles the very tegument of the metacercaria it is harboring. The wall
is comprised of a spongy matrix of tissue interspersed with dense nuclei
and a very thin granular outer border.

Figure 1

Figure 2

Figure 3

Figure 4

Definitions

Acetabulum: The
ventral sucker on a trematode worm.

Amnicolid
and Hydrobiid: fresh or brackish water snails belonging to the family
Hydrobiidae which are characterized by true gills and opercula, versus
pulmonate, or air-breathing, structures.

Cercarial: The last
larval stage of trematodes, free swimming, from the first intermediate
host, to the second intermediate host, where penetration of that host
occurs.

Creationism: The
belief that God created all things as described in Genesis.

Cyprinodont: the
killifish family of fresh and saltwater minnows.

Digenetic: Subclass
Digenea, parasitic worms, a subclass of the Trematoda, having two or more
asexual generations, an alternation of hosts, the first almost always
a mollusc, and which are endoparasitic in vertebrates such as birds.

Evolutionism: the
belief that all life forms arose over millions of years from a common
ancestor due to mutations in the genetic code and a stochastic system
of selection called Natural Selection.

Trematode: Class
Trematoda of helminths which are parasitic flatworms (flukes) mainly in
the digestive tract of all classes of vertebrates. These trematodes possess
a digestive tract, specialized sensory organs, and muscular sucking disks
which serve to attach the fluke to the host.

Appendix

Biological tissues
such as Ascocotyle cysts must be processed properly in order to
be viewed in an electron microscope. First, the tissue of interest must
be dissected and chemically processed in fixative, buffers, and alcohols
(Lumsden, 1970). Then it must be embedded in a liquid polymer that will
harden upon heating (Figures 56). Once hardened, the tissues can
be thin sectioned on an ultramicrotome (Figure 7: blade and tissue block
shown). Finally, tissue sections are transferred to thin metal grids on
which they are stained with metal salts and placed into a special chamber
in the TEM (Figures 89).

Figure 5

Figure 6

Figure 7

Figure 8

Figure 9

Acknowledgments

The author thanks
Ronnie Palmer of the Gulf Coast Research Laboratory for specimens, Les
Eddington of Azusa Pacific University for technical assistance and for
reviewing a preliminary draft of this paper, George Howe for critical
comments and support of the project, and Patrick Armitage for illustrations.
The author is also indebted to the reviewers for comments.

References

CRSQ: Creation
Research Society Quarterly

JP: Journal of
Parasitology

Aeby, G. 1991. Behavioral
and ecological relationships of a parasite and its hosts within a coral
reef system. Pacific Science 45(3):263269.

.
1960. Studies on helminth parasites from the Coast of Florida II. Digenetic
trematodes from shore birds of the west coast of Florida. Bulletin
of Marine Science of the Gulf and Caribbean 10(1):4054.

.
1963b. A new heterophyid trematode of the Ascocotyle complex of
species encysted in poeciliid and cyprinodont fishes of southeast Texas.
Proceedings of the Helminthological Society of Washington 30:293296.

Schroeder, R. and
W. H. Leigh. 1965. The life history of Ascocotyle pachycystis sp.
n., a trematode from the racoon in South Florida. JP 51:591599.

Skinner, R. 1975.
Parasites of the striped mullet, Mugil cephalus, from Biscayne
Bay, Florida with descriptions of a new genus and three new species of
trematodes. Bulletin of Marine Science 25:318345.

So, F. W. and D.
D. Wittrock. 1982. Ultrastructure of the metacercarial cyst of Ornithodiplostomum
ptychocheilus (Trematoda:Diplostomatidae) from the brains of fathead
minnows. Transactions of the American Microscopical Society 101(2):181185.

Sogandares-Bernal,
F. and J. F. Bridgman. 1960. Three Ascocotyle complex trematodes
(Heterophyidae), encysted in fishes from Louisiana including the description
of a new genus. Tulane Studies in Zoology 8(2):3139.

Sogandares-Bernal,
F., and R. D. Lumsden. 1963. The generic status of the heterophyid trematodes
of the Ascocotyle complex, including notes on the systematics and
biology of the Ascocotyle angrense Travassos 1916. JP 49:264274.